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Path Pro 2023 > Inflammation > Flashcards

Inflammation Flashcards

1
Q

What is inflammation?

A

Response of living tissue to injury

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2
Q

Acute inflammation features

A 
Immediate
Short
Limits damage
Innate (built in)
Stereotyped - same response each time
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3
Q

Phases of inflammation and aims

A

Vascular phase - changes blood flow, accumulates exudate

Cellular phase - delivers neutrophils

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4
Q

How is inflammation controlled

A

Chemical mediators

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5
Q

What’s an cause inflammation

A

Trauma/foreign body
Microorganisms
Hypersensitivity (allergies)
Other illness (cancer, necrosis)

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6
Q

5 clinical signs of inflammation

A 
Rubor (red)
Calor (hot)
Dolor (pain)
Tumor (swelling)
Loss of function
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7
Q

Vascular changes in vascular phase and what they achieve

A 
Vasoconstriction (seconds)
Vasodilation (minutes) (redness and heat)
Increased permeability (swelling)
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8
Q

Starlings law

A

Movement of fluid is controlled by:
Hydrostatic pressure and oncotic pressure

(High hydrostatic pressure pushes fluids out, high oncotic pressure pulls fluid in - sponge)

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9
Q

What do the vascular changes achieve?

A

Vasodilation - increased capillary hydrostatic pressure

Increased vessel permeability - plasma proteins move to interstitium (increases interstitial oncotic pressure)

FLUID MOVES OUT OF VESSEL INTO INTERSTITIUM = OEDEMA

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10
Q

What happens as a result of fluid moving out of capillaries/vessels?

A

Increased viscosity of blood

Reduced flow = stasis

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11
Q

Exudate (how and what is it)

A

Caused by increased vascular permeability
Protein rich
Occurs in inflammation

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12
Q

Transudate (how and what)

A

Permeability unchanged
Movement due to - increased capillary hydrostatic pressure/reduced capillary oncotic pressure

Occurs in: heart, hepatic, renal failure

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13
Q

How does a vessel wall become permeable? (3 ways)

A

Retraction of endothelial cells (histamine, nitric oxide, leukotrienes)

Direct injury (burns, toxins, trauma)

Leukocyte dependent injury (enzymes/toxic oxygen species released by active inflammatory cells)

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14
Q

Why is the vascular phase effective? (3 ways)

A

Interstitial fluid increase dilutes toxins

Exudate delivers proteins (fibrin limits spread via mesh prison, immunoglobulins delivered)

Fluid drains to lymph nodes (delivers antigens - stimulate adaptive response)

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15
Q

Main cell involved in cellular phase

A

Neutrophil - trilobed nucleus (appear purple dots on histology)

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16
Q

How do neutrophils escape vessels (4 stages)

A

Margination - move to periphery of vessel

Rolling - via selectins

Adhesion - via integrins

Emigration (diapedesis) - moves to interstitium

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17
Q

How do selectins work?

A

Present on activated endothelial cells
Activated by chemical mediators
Responsible for ROLLING

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18
Q

How do integrins work?

A

Present on neutrophil surface
Change from low affinity to high affinity
Responsible for ADHESION

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19
Q

How do neutrophils move through interstitium?

A

Chemotaxis - Movement along an increasing chemical gradient (low —> high) of chemoattractants

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20
Q

Chemoattractants: and what it achieves

A

Bacterial peptides, inflammatory mediators

Causes rearrangement of neutrophil cytoskeleton to propel itself forward

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21
Q

What do neutrophils do?

A

Phagocytosis
Into vesicle = phagosome
Fuse with lysosomes = phagolysosome
Release lysozymes and digest —> exocytosis

Also release inflators mediators

22
Q

How do neutrophils recognise what to phagocytose?

A

Opsonins on pathogen - C3b, Fc

Receptors for C3b and Fc are on neutrophil surface

23
Q

Killing mechanisms of neutrophils

A

Oxygen dependent - ROS ( superoxide, hydroxyl, hydrogen peroxide) or RNS (nitric oxide, nitrogen dioxide)

Oxygen independent - lysozyme, hydrolytic enzymes, defensins

24
Q

Why is the cellular phase effective?

A

Removes pathogens and necrotic tissue

Releases inflammatory mediators

25
Q

What are inflammatory mediators

A

Chemical messengers - control and coordinate inflammatory response

26
Q

Where can inflammatory mediators arise from

A

Activated inflammatory cells
Platelets
Endothelial cells
Toxins (chemoattractants)

27
Q

Inflammatory mediators that cause vasodilation

A

Histamine
Serotonin
Prostaglandins
Nitric oxide

28
Q

Inflammatory mediators that increase permeability

A

Histamine
Bradykinin
Leukotrienes
C3a, C5a

29
Q

Mediators that act as chemoattractants

A

C5a
TNF - a
IL - 1
Bacterial peptides

30
Q

Inflammatory mediators that cause fever

A

Prostaglandins
IL-1
IL-6
TNF-a

31
Q

Inflammatory mediators that cause pain

A

Bradykinin
Substance P
Prostaglandins

32
Q

Complications of inflammation can be:

A

Local (tissue, organ) or systemic (whole body)

33
Q

Local complications (SELP)

A

Swelling - compression of tubes (airways, bile duct, intestines)

Exudate - compress organs (cardiac tamponade in pericardial sac)

Loss of fluid - burns = dehydration

Pain - muscle atrophy., psychosocial effects

34
Q

Systemic complications

A

Fever - pyrogens act on hypothalamus (eg prostaglandins)

Leucocytosis - increased white cell production (act on bone marrow IL-6, TNF-a)

Acute phase response

Septic shock

35
Q

Acute phase response and proteins

A

Malaise, reduced appetite, altered sleep, tachycardia
Induces rest

Proteins:
C reactive protein (CRP= inflammation severity marker)
Fibrinogen
A1 antitrypsin

36
Q

Septic shock

A 
Huge release of chemical mediators 
Wide spread VASODILATION 
Hypotension
Tachycardia 
Multi organ failure 
FATAL
37
Q

After acute inflammation

A

Resolution
Repair with connective tissue
Chronic inflammation

38
Q

Complete resolution

A

Mediators have short half lives
Vessel and permeability return to normal
Neutrophils = apoptosis and phagocytosed
Exudate drains into lymphatics
Regeneration of tissue if architecture is preserved

39
Q

Repair with connective tissue

A

Fibrosis if substantial tissue destruction

40
Q

Chronic inflammation

A

Prolonged inflammation with repair

41
Q

Itis =

A

Inflammation

42
Q

appendicitis cause

A

Blocked lumen from faecolith (solid poo)
Accumulation of bacteria and exudate
Increased pressure can cause burst appendix

43
Q

Appendicitis symptoms

A

Vague abdominal pain
Sharp tight lower right fossa pain
Severe overall pain

44
Q

Cause and symptoms pneumonia

A

Streptococcus pneumoniae
Haemophilus influenzae

Shortness of breath
Cough
Yellow/green sputum
Fever

45
Q

Risk factors pneumonia

A

Smoking

Pre existing lung condition (COPD, asthma, malignancy)

46
Q

Bacteria meningitis causes and symptoms

A

Cause:
Group B streptococcus
E.coli
Neisseria meningitides

Symptoms/signs:
Headache
Neck stiffness
Photophobia (bright lights)
Altered mental state
47
Q

What happens during meningitis?

A

Inflammation of meninges (protective layers between skull and brain)

DURA, ARACHNOID, PIA (mater) - layers

Compression of brain occurs

48
Q

Abscess

A

Accumulation of dead and dying neutrophils (pus)
Liquefactive necrosis
Compression of surrounding structures

49
Q

Inflammation of serous cavities

A

Pleural, peritoneal, pericardium

50
Q

Disorders of acute inflammation

A

Hereditary angio-oedema
Alpha-1 antitrypsin deficiency
Chronic granulomatous disease

Path Pro 2023 (21 decks)

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